Abstract
BACKGROUND AND AIM: Prenatal exposure to air pollution including particulate matter (PM), NO2, and SO2, has been linked with attention deficit hyperactivity disorder (ADHD) in children. Epigenetic influence has been suggested to have a role in the association between exposure to air pollution and ADHD. We aimed to investigate the epigenetic effects on the association between prenatal air pollution exposure and ADHD symptoms in children. METHODS: Whole blood samples of 60 children were obtained at age 2 and 6 years repeatedly and genome-wide DNA methylation was analyzed using the Illumina Infinium Human Methylation BeadChip 450K. After quality control, a total of 256,864 CpG sites were analyzed for their association with prenatal PM10, PM2.5, NO2, and SO2 exposure in the first, second, and third trimesters of pregnancy, respectively. CpG sites associated with prenatal air pollution exposure were studied in relation to ADHD rating scale (ARS) scores at ages 6 and 8. We aimed to investigate the epigenetic effects on the association between prenatal air pollution exposure and ADHD symptoms in children. RESULTS:DNA methylation levels at the 6 CpG sites at age 2 were associated with prenatal SO2 exposure levels at the third trimester: CpG sites located in GP1BB, ATP2C2, GNB4, GRIA1, RPE, INPP5D. Among these, 1 IQR increase in the methylation of cg14130977 (GP1BB) and cg16698748 (ATP2C2) at age 2 was associated with a 0.11 (95% confidence interval (CI) 0.41, 0.83) and 0.12 (95% CI 0.3, 0.76) increase in ARS at age 6, respectively. cg21656520 (RPE) and cg22331159 (INPP5D) showed similar results. CONCLUSIONS:Changes in DNA methylation levels at the CpG sites associated with prenatal SO2 exposure led to increases in ARS scores, suggesting that epigenetic mechanisms underly the effects of prenatal exposure to air pollution on ADHD symptoms in children. KEYWORDS: prenatal, sulfur dioxide, SO2, DNA methylation, ADHD, epigenome-wide association study, epigenetics
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